Cyclosporin H (CsH), a specific inhibitor of FPR1, inhibited lung inflammation in the ALI models. CsH significantly attenuated MTDs or NFP-induced inflammatory lung injury and activation of MAPK and AKT pathways. Cyclosporin H is a viral transduction enha

Cyclosporin H is a potent inhibitor of FMLP-induced superoxide anion (O2-) formation in human neutrophils. Cyclosporin H inhibited FMLP binding in HL-60 membranes with a Ki (inhibition constant) of 0.10 μM. Cyclosporin H inhibited activation by FMLP of high affinity GTPase (the enzymatic activity of alpha-subunits of heterotrimeric regulatory guanine nucleotide-binding proteins) in HL-60 membranes with a Ki of 0.79 μM. Cyclosporin H inhibited the stimulatory effects of FMLP on cytosolic Ca2+ concentration ([Ca2+]i), O2- formation, and beta-glucuronidase release with Ki values of 0.08, 0.24, and 0.45 μM, respectively.

Cyclosporin H, administered intraperitoneally (i.p.) at a dosage of 5 mg/kg prior to challenge with LPS or HCl, mitigates lung injury caused by LPS or HCl in a lung injury model.